I. Field of the Invention
The present invention relates generally to the field of cardiac rhythm management devices, including atrial, ventricular, and dual chamber pacemakers. More specifically, the present invention relates to a portion of the sensing circuit of the cardiac rhythm management device that may be utilized during capture verification. The sensing circuit of the present invention includes a band pass filter having a single high pass pole and a sense amplifier electrically coupled within the cardiac rhythm management device. The sense amplifier is electrically coupled in a manner, wherein a polarity of an amplitude of a sensed signal corresponding to an evoked response is opposite a polarity of an amplitude of a sensed signal corresponding to afterpotential.
II. Discussion of the Prior Art
Regardless of the type of cardiac rhythm management device that is employed, all operate to stimulate excitable heart tissue cells adjacent to the electrode of the lead coupled to the rhythm management device. Response to myocardial stimulation or "capture" is a function of the positive and negative charges found in each myocardial cell within the heart. More specifically, the selective permeability of each myocardial cell works to retain potassium and exclude sodium such that, when the cell is at rest, the concentration of sodium ions outside of the cell membrane is approximately equal to the concentration of potassium ions inside the cell membrane. However, the selective permeability also retains other negative particles within the cell membrane such that the inside of the cell membrane is negatively charged with respect to the outside when the cell is at rest.
When a stimulus is applied to the cell membrane, the selective permeability of the cell membrane is disturbed and it can no longer block the inflow of sodium ions from outside the cell membrane. The inflow of sodium ions at the stimulation site causes the adjacent portions of the cell membrane to lose its selective permeability, thereby causing a chain reaction across the cell membrane until the cell interior is flooded with sodium ions. This process, referred to as depolarization, causes the myocardial cell to have a net positive charge due to the inflow of sodium ions. The electrical depolarization of the cell interior causes a mechanical contraction or shortening of the myofibrils of the cell membrane. The syncytial structure of the myocardium will cause the depolarization originating in any one cell to radiate through the entire mass of the heart muscle so that all cells are stimulated for effective pumping. Following heart contraction or systole, the selective permeability of the cell membrane returns and sodium is pumped out until the cell is re-polarized with a negative charge within the cell membrane. This causes the cell membrane to relax and return to the fully extended state, referred to as diastole.
In a normal heart, the sino-atrial (SA) node initiates the myocardial stimulation described above. The SA node comprises a bundle of unique cells disposed within the roof of the right atrium. Each cell membrane of the SA node has a characteristic tendency to leak sodium ions gradually over time such that the cell membrane periodically breaks down and allows an inflow of sodium ions, thereby causing the SA node cells to depolarize. The SA node cells are in communication with the surrounding atrial muscle cells such that the depolarization of the SA node cells causes the adjacent atrial muscle cells to depolarize. This results in atrial systole wherein the atria contract to empty blood into the ventricles. The atrial depolarization from the SA node is detected by the atrioventicular (AV) node which, in turn, communicates the depolarization impulse into the ventricles via the Bundle of His and Purkinje fibers following a brief conduction delay.
In this fashion, ventricular systole lags behind atrial systole such that the blood from the ventricles is pumped through the body and lungs after being filled by the atria. Atrial and ventricular diastole follow wherein the myocardium is repolarized and the heart muscle relaxes in preparation for the next cardiac cycle. It is when this system fails or functions abnormally that a cardiac rhythm management device may be needed to deliver an electronic pacing stimulus to the heart so as to maintain proper heart rate and synchronization of the filling and contraction of the atrial and ventricular chambers of the heart.
The success of a cardiac rhythm management device in causing a depolarization or evoking a response hinges on whether the energy of the pacing stimulus as delivered to the myocardium exceeds a threshold value. This threshold value, referred to as the capture threshold, represents the amount of electrical energy required to alter the permeability of the myocardial cells to thereby initiate cell depolarization. If the energy of the pacing stimulus does not exceed the capture threshold, then the permeability of the myocardial cells will not be altered and thus no depolarization will result. If, on the other hand, the energy of the pacing stimulus exceeds the capture threshold, then the permeability of the myocardial cells will be altered such that depolarization will result.
Changes in the capture threshold may be detected by monitoring the efficacy of stimulating pulses at a given energy level. If capture does not occur at a particular stimulation energy level which previously was adequate to effect capture, then it can be surmised that the capture threshold has increased and that the stimulation energy should be increased. On the other hand, if capture occurs consistently at a particular stimulation energy level over a relatively large number of successive stimulation cycles, then it is possible that the capture threshold has decreased such that the stimulation energy is being delivered at a level higher than necessary to effect capture. This can be verified by lowering the stimulation energy level and monitoring for loss of capture at the new energy level.
The ability to detect capture in a cardiac rhythm management device is extremely desirable in that delivering stimulation pulses having energy far in excess of the patient's capture threshold is wasteful of the cardiac rhythm management device's limited power supply. In order to minimize current drain on the power supply, it is desirable to automatically adjust the cardiac rhythm management device such that the amount of stimulation energy delivered to the myocardium is maintained at the lowest level that will reliably capture the heart. To accomplish this, a process known as "capture verification" must be performed wherein the cardiac rhythm management device monitors to determine whether an evoked response or R-wave occurs in the heart following the delivery of each pacing stimulus pulse.
For the most part, prior art implantable cardiac rhythm management devices, including bradycardia and tachycardia pacemakers and cardiac defibrillators, have sense amplifier circuits for amplifying and filtering electrogram signals sensed through electrodes placed in or on the heart and which are coupled by suitable leads to the implantable cardiac rhythm management device. The signals emanating from the sense amplifier are applied to one input of a comparator circuit whose other input is connected to a reference potential. Only when an electrogram signal from the sense amplifier exceeds the reference potential threshold will it be treated as an evoked response. The source reference potential may be referred to as a sensing threshold. In some instances the amplitude of pacing artifact may be so great that it becomes difficult to distinguish the amplitude corresponding to an evoked response with the amplitude corresponding to artifact. Hence, there is a need for a capture verification circuit of a cardiac rhythm management device capable of differentiating between the amplitude corresponding to evoked response and the amplitude corresponding to artifact of a sensed signal. There is a further need for a capture verification circuit suitable for use with either unipolar or bipolar stimulation and which does not depend upon lead placement. These and numerous other disadvantages of the prior art necessitates the need for the method and apparatus provided by the present invention.